Solid tumors can survive hypoxic condition (the high cell density of a tumor limits the availability of oxygen to cells) by using protective mechanisms including the activation of hypoxia-inducible factor-1α (HIF-1α) a transcription factor that induces, among others, antiapoptotic Bcl2, multidrug resistance (MDR), VEGF gene expression, and reprogramming of glucose metabolism that account for cell proliferation, angiogenesis, and chemoresistance [1]. The gene discussed is BCL2; the disease is neoplasm.